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Fucoidan induces G1 phase arrest and apoptosis through caspases-dependent pathway and ROS induction in human breast
Amal M Banafa1, Sadia Roshan1, Yun-Yi Liu1
1The Genetic Engineering International Cooperation Base of Ministry of Science and Technology, Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, 430074, China.
Abstract:
Fucoidan is an active component of seaweed, which inhibits proliferation and induces apoptosis of several tumor cells while the detailed mechanisms underlying this process are still not clear. In this study, the effect of Fucoidan on the proliferation and apoptosis of human breast cancer MCF-7 cells and the molecular mechanism of Fucoidan action were investigated. Viable cell number of MCF-7 cells was decreased by Fucoidan treatment in a dose-dependent manner as measured by MTT assay. Fucoidan treatment resulted in G1 phase arrest of MCF-7 cells as revealed by flow cytometry, which was associated with the decrease in the gene expression of cyclin D1 and CDK-4. Annexin V/PI staining results showed that the number of apoptotic cells was associated with regulation of cytochrome C, caspase-8, Bax and Bcl-2 at transcriptional and translational levels. Both morphologic observation and Hoechst 33258 assay results confirmed the pro-apoptotic effect of Fucoidan. Meanwhile, the ROS production was also increased by Fucoidan treatment, which suggested that Fucoidan induced oxidative damage in MCF-7 cells. The results of present study demonstrated that Fucoidan could induce G1 phase arrest and apoptosis in MCF-7 cells through regulating the cell cycle and apoptosis-related genes or proteins expression, and ROS generation is also involved in these processes.
Insights
Fucoidan, a seaweed component, inhibits human breast cancer cell (MCF-7) proliferation and induces apoptosis by arresting cells in the G1 phase. This process involves regulating cell cycle and apoptosis-related genes and proteins, with reactive oxygen species (ROS) playing a role.
Area of Science:
- Marine Biotechnology
- Cancer Biology
- Molecular Pharmacology
Background:
- Fucoidan, derived from seaweed, exhibits anti-cancer properties against various tumor cells.
- The precise molecular mechanisms by which fucoidan inhibits cancer cell proliferation and induces apoptosis remain incompletely understood.
Purpose of the Study:
- To investigate the effects of fucoidan on the proliferation and apoptosis of human breast cancer MCF-7 cells.
- To elucidate the molecular mechanisms underlying fucoidan's action in these cells.
Main Methods:
- MTT assay to assess cell viability.
- Flow cytometry for cell cycle analysis (G1 phase arrest).
- Annexin V/PI staining, Western blotting, and gene expression analysis for apoptosis markers (cytochrome C, caspase-8, Bax, Bcl-2).
- Hoechst 33258 staining and morphological observation for apoptosis confirmation.
- Measurement of reactive oxygen species (ROS) production.
Main Results:
- Fucoidan significantly decreased MCF-7 cell viability in a dose-dependent manner.
- Fucoidan induced G1 phase arrest, correlating with decreased cyclin D1 and CDK-4 expression.
- Apoptosis was confirmed through morphological changes, Hoechst staining, and modulation of apoptosis-related proteins and genes (cytochrome C, caspase-8, Bax, Bcl-2).
- Fucoidan treatment increased ROS production, indicating oxidative damage.
Conclusions:
- Fucoidan effectively induces G1 phase arrest and apoptosis in human breast cancer MCF-7 cells.
- These effects are mediated by the regulation of cell cycle and apoptosis-related genes and proteins.
- Reactive oxygen species (ROS) generation is implicated in the fucoidan-induced anti-cancer effects.
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